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Emilio Casanova

Current basic questions of mouse models aim towards the question which mutations cooperate in the development of different types of cancer. One concept requires state of the art cancer models to explore the combination of conventional with targeted therapies. Emilio Casanova has extensive expertise in the generation of modern murine models of neoplastic disease, including the Multi-hit mouse, which allows for the evaluation of oncogene cooperativities in tumor development. The model is based on the stochastic expression of oncogene combinations ('hits') that are mediated by Cre in a given tissue. Cells with cooperating hits are positively selected and give rise to tumors. We used this approach to evaluate the requirement of Ras downstream effector pathways in tumorigenesis. Moreover, the Casanova group has two industrial project collaborations.

About Emilio Casanova

Since 2014 he is Professor for "Transgenic Models in Cancer Research" at the Medical University Vienna.

He is an expert in the generation of genetically modified mice and as of 2017 he has more than 57 PubMed based publications with an excess of 3.500 citations and an h-index of 24 according to his google scholar profile. He serves continuously as reviewer for internationally reputed journals. In addition to the funding of the LBG and partner institutions towards the LBI-CR, he has been responsible to obtain more than 1.5 M€ of external funding towards his research.

EC was PhD student with Pedro Calvo and Miguel Chinchetru at the Department of Biochemistry and Molecular Biology, University of Leon, Spain. He did post-doctoral research at the German Cancer Research Center in Heidelberg with Günther Schütz and at the Biozentrum in Basel with Bernhardt Bettler. Since 2006 he runs his individual research group at the LBI-CR.

Lung cancer is leading the worldwide cancer related deaths. It can be divided into to two main types: Small Cell Lung Cancer (SCLC) and Non-Small Cell Lung Cancer (NSCLC), the later accounting for 80% of the cases. Common genetic alterations associated with lung cancer are the loss of tumor suppressors, like p53, LKB1 etc. and activating mutations, overexpression, amplification of oncogenes, such EGFR and K-RAS. In lung tumors, EGFR signals through K-RAS, PI3K and STAT3.

AKT/PKB is a family of serine-threonine kinases activated in response to growth stimuli downstream of the PI3K /PTEN pathway. The AKT family consists of three members: AKT-1, AKT-2 and AKT-3, and has been implicated in different malignancies, such as glioblastoma, ovarian, gastric, colorectal, prostate and breast tumors. Gene amplification and/or over-activation of the three AKT members have been found in different tumors.

Liver fibrosis constitutes a considerable health problem in the human population. In order to further understand the molecular mechanisms underlying liver fibrogenesis it is mandatory to generate genetic mouse models closely resembling human disease development and progression.

Recombinant protein production in eukaryotic cells is one of the main topics of biotechnology. One of the most critical steps is the development of appropriate vectors to express the protein of interest. Bacterial Artificial Chromosomes (BACs) containing the appropriate locus can be used as expression vectors in the protein production field. In collaboration with Dr. A. Bauer, we have developed a BAC-based vector system that improves the protein production by a factor of 10 when compared to a conventional vector in stable HEK293 cell lines.